Conduction deficits and membrane disruption of spinal cord axons as a function of magnitude and rate of strain.

White matter strips extracted from adult guinea pig spinal cords were subjected to tensile strain (stretch) injury ex vivo. Strain was carried out at three magnitudes (25, 50, and 100%) and two strain rate regimens: slow (0.006-0.008 s(-1)) and fast (355-519 s(-1)). The cord samples were monitored physiologically using a double sucrose-gap technique and anatomically using a horseradish peroxidase assay. It seems that a higher magnitude of strain inflicted significantly more functional and structural damage within each strain rate group. Likewise, a higher strain rate inflicted more damage when the strain magnitude was maintained. It is evident that axons have remarkable tolerance to strain injury at a slow strain rate. Even a 100% strain at the slow rate only eliminated two-thirds of the compound action potential amplitude and resulted in almost no membrane damage when examined 30 min after strain. It is also clear that the spontaneous recovery is evident yet not complete compared with preinjury levels at the fast strain rate. To examine the factors that might influence the vulnerability of axons to strain, we have shown that the axonal diameters did not play a significant role in dictating the susceptibility of axons to strain. Rather, it is speculated that the location of axons might be a more important factor in this regard. The knowledge gained from this study is likely to be informative in elucidating the spinal cord biomechanical response to strain and strain rate.